3 months; P=0.014) and PCI grade (grade I, 25.6 months; grade II and III, 16.3 months; P=0.023). Conclusions The feasibility of IP paclitaxel and systemic chemotherapy administration was demonstrated in this experience-based retrospective analysis suggesting that the procedure is beneficial in patients with PM of AGC. Purpose Patients with pathological stage T1N+ or T2-3N0 gastric cancer may experience disease recurrence following curative gastrectomy. However, the current Japanese Gastric Cancer Treatment Guidelines do not recommend postoperative adjuvant chemotherapy for such patients. This study aimed to identify the prognostic factors for patients with pT1N+ or pT2-3N0 gastric cancer using a multi-institutional dataset. Materials and Methods We retrospectively analyzed the data obtained from 401 patients with pT1N+ or pT2-3N0 gastric cancer who underwent curative gastrectomy at 9 institutions between 2010 and 2014. Results Of the 401 patients assessed, 24 (6.0%) experienced postoperative disease recurrence. Multivariate analysis revealed that age ?70 years (hazard ratio [HR], 2.62; 95% confidence interval [CI], 1.09-7.23; P=0.030) and lymphatic and/or venous invasion (lymphovascular invasion (LVI) HR, 7.88; 95% CI, 1.66-140.9; P=0.005) were independent prognostic factors for poor recurrence-free survival. https://www.selleckchem.com/products/atglistatin.html There was no significant association between LVI and the site of initial recurrence. Conclusions LVI is an indicator of poor prognosis in patients with pT1N+ or pT2-3N0 gastric cancer. Purpose Gastrointestinal stromal tumors (GISTs) frequently harbor activating gene mutations in either KIT or platelet-derived growth factor receptor A (PDGFRA) and are highly responsive to several selective tyrosine kinase inhibitors. In this study, a targeted next-generation sequencing (NGS) assay with an Oncomine Focus Assay (OFA) panel was used for the genetic characterization of molecular targets in 30 Korean patients with GIST. Materials and Methods Using the OFA that enables rapid and simultaneous detection of hotspots, single nucleotide variants (SNVs), insertion and deletions (Indels), copy number variants (CNVs), and gene fusions across 52 genes relevant to solid tumors, targeted NGS was performed using genomic DNA extracted from formalin-fixed and paraffin-embedded samples of 30 GISTs. Results Forty-three hotspot/other likely pathogenic variants (33 SNVs, 8 Indels, and 2 amplifications) in 16 genes were identified in 26 of the 30 GISTs. KIT variants were most frequent (44%, 19/43), followed by 6 variants in PIK3CA, 3 in PDGFRA, 2 each in JAK1 and EGFR, and 1 each in AKT1, ALK, CCND1, CTNNB1, FGFR3, FGFR4, GNA11, GNAQ, JAK3, MET, and SMO. Based on the mutation types, majority of the variants carried missense mutations (60%, 26/43), followed by 8 frameshifts, 6 nonsense, 1 stop-loss, and 2 amplifications. Conclusions Our study confirmed the advantage of using targeted NGS with a cancer gene panel to efficiently identify mutations associated with GISTs. These findings may provide a molecular genetic basis for developing new drugs targeting these gene mutations for GIST therapy. Gastrectomy with lymph node dissection remains the gold standard for curative treatment of gastric cancer. Dissection of splenic hilar lymph nodes has been included as a part of D2 lymph node dissection for proximal gastric cancer. Previously, pancreatico-splenectomy has been performed for dissecting splenic hilar lymph nodes, followed by pancreas-preserving splenectomy and spleen-preserving lymphadenectomy. However, the necessity of routine splenectomy or splenic hilar lymph node dissection has been under debate due to the increased morbidity caused by splenectomy and the poor prognostic feature of splenic hilar lymph node metastasis. In contrast, the relatively high incidence of splenic hilar lymph node metastasis, survival advantage, and therapeutic value of splenic hilar lymph node dissection in some patient subgroups, as well as the effective use of novel technologies, still supports the necessity and applicability of splenic hilar lymph node dissection. In this review, we aimed to evaluate the need for splenic hilar lymph node dissection and suggest the subgroup of patients with favorable outcomes. Splenic hilar lymph node dissection has been the standard treatment for advanced proximal gastric cancer. Splenectomy is typically performed as part of this procedure. However, splenectomy has some disadvantages, such as increased risk of postoperative complications, especially pancreatic fistula. Moreover, patients who underwent splenectomy are vulnerable to potentially fatal infection caused by encapsulated bacteria. Furthermore, several studies have shown an association of splenectomy with cancer development and increased risk of thromboembolic events. Therefore, splenectomy should be avoided if it does not confer a distinct oncological advantage. Most studies that compared patients who underwent splenectomy and those who did not failed to demonstrate the efficacy of splenectomy. Based on the results of a randomized controlled trial conducted in Japan, prophylactic dissection with splenectomy is no longer recommended in patients with gastric cancer with no invasion of the greater curvature. However, patients with greater curvature invasion or those with remnant gastric cancer still need to undergo splenectomy to facilitate splenic hilar node dissection. Spleen-preserving splenic hilar node dissection is a new procedure that may help delink splenic hilar node dissection and splenectomy. In this review, we examine the evidence pertaining to the efficacy and disadvantages of splenectomy. We discuss the possibility of spleen-preserving surgery for prophylactic splenic hilar node dissection to overcome the disadvantages of splenectomy. Type 2 diabetes is associated with adverse central nervous system effects, including a doubled risk for Alzheimer's disease (AD) and increased risk of cognitive impairment, but the mechanisms connecting diabetes to cognitive decline and dementia are unknown. One possible link between these diseases may be the associated alterations to cholesterol oxidation and metabolism in the brain. We will survey evidence demonstrating alterations to oxysterols in the brain in AD and diabetes and how these oxysterols could contribute to pathology, as well as identifying research questions that have not yet been addressed to allow for a fuller understanding of the role of oxysterols in AD and diabetes. © 2019 The Author(s).